Download
slide1 n.
Skip this Video
Loading SlideShow in 5 Seconds..
Case PowerPoint Presentation

Case

193 Vues Download Presentation
Télécharger la présentation

Case

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  1. Case • 28y male involved in an industrial accident • Sustained significant injuries to right lower leg, femur and ?hemipelvis • Prolonged extrication “tons of blood” at the scene

  2. Case 1 • Looks very unwell with ++ ongoing bleeding • GCS E3 V4 M5 (12) • Temp 34.7 • HR 160 • BP 77/50 manual • RR 30 • SaO2 97% 10L by mask • What is your initial management?

  3. Case • What other investigations? • Who are you going to call? • Surgery and IR are held up for 30min • Is there anything else we can do?

  4. Massive transfusion (all bleeding stops…) Grand Rounds Oct 2nd 2008 Kristian Hecht PGY-3 CCFP-EM

  5. Objectives • Define massive transfusion • Review complications of massive transfusion • Review FMC’s Massive Transfusion Protocol • Review literature supporting the MTP • Review adjunctive therapies in massive hemorrhage

  6. Background • First attempted blood transfusion was in 1492 after Pope Innocent VIII became comatose • Blood from 3 aides was instilled into the Pope’s mouth • All 4 died

  7. Background • In 1600’s many animal-to-human transfusions attempted • These were later banned due to high mortality • The first documented successful transfusion was between two dogs in 1667 • The first documented human-to-human transfusion was in 1818 by Dr. James Blundell a British obstetrician

  8. Background • Hemorrhage is the second leading cause of death in trauma • CNS injury is 1st • May require massive transfusion

  9. Background • Massive transfusion (MT): • >10U pRBC’s in 24h • Replacement of 50% blood volume in 3h • 4U pRBC in 4h with ongoing major bleeding • Replacement with blood loss >150mL/min • Required in only 1% of civilian trauma pts • Mortality rates are between 20 – 50% in those requiring massive transfusion

  10. Complications of MT • Acute hemolytic transfusion reactions • Hyperkalemia • Acidosis • Hypothermia • Hypocalcemia • Coagulopathy • All more common and/or severe with increasing number of units transfused

  11. Acute hemolytic reactions • Most often due to ABO incompatible RBC’s or plasma (clerical error, lab error etc) • Rarely seen with unmatched O+ pRBC’s • Occasionally with unmatched type specific pRBC’s • Commonly with unmatched type specific whole blood

  12. Hyperkalemia • Storage of pRBC’s results in cell lysis and increased extracellular [K+] • 12 mEq/L at 7d • 32 mEq/L at 21d

  13. Hyperkalemia • Inconsequential if infused slowly • K+ is shifted to intracellular space and later eliminated • If large amounts of pRBC’s infused through a central line a large amount of K+ is delivered directly to the RA • Potentially resulting in…

  14. Hyperkalemia • If encountered treat as per medical hyperkalemia • May be prevented by using peripheral venous access • Use of fresh blood (<14d) may decrease incidence

  15. Hypothermia • Traumatized pts are at risk for significant hypothermia due to environmental and surgical exposure • pRBC’s are stored at 4°C and will cause rapid hypothermia if not put through warmer • Hypothermia is an independent risk factor for mortality in trauma

  16. Hypothermia • Physiologic effects: • Decreased contractility • Cardiac dysrhythmia • Coagulopathy

  17. Hypothermia • Treatment • Drapes/blankets • Warmed IV fluids • Warm humidified O2 • External rewaming (hot air blankets, etc) • Internal rewarming (peritoneal/pleural lavage)

  18. QTc =510

  19. Hypocalcemia • Citrate is used as an anticoagulant in all blood products • Citrate binds ionized calcium and inhibits calcium-dependent coagulation • Higher concentrations in FFP and Plts • Usually inconsequential due to rapid hepatic metabolism • May become significant with poor circulation and/or large amounts

  20. Hypocalcemia • Tetany • QT prolongation • Decreased myocardial contractility • Hypotension • Exacerbation of concomitant hyperkalemia • Coagulopathy (occurs at very low [Ca2+])

  21. Hypocalcemia • Treatment • Correct shock • Decrease rate of blood product infusion • IV CaCl2 1g slowly

  22. Acidosis • In hemorrhagic shock metabolic acidosis results from poor perfusion and subsequent lactate production • Stored pRBC’s pH 6.87at 21d • Metabolism of exogenous acid may be decreased due to poor circulation or rapid/large amount

  23. Acidosis • Causes other electrolyte disturbances (hyper K+) • Independent risk factor for coagulopathy • Activity of factor VIIa decreases by 90% when pH drops from 7.4 to 7.0

  24. Acidosis • Treatment • Correction of volume status and restoration of tissue perfusion • Use fresh blood products if possible • Addition of HCO3- is ineffective

  25. pH 6.87 [K+] 32 mEq/L 4°C citrate Stored blood products

  26. Coagulopathy • Clinically • Oozing from IV sites, wounds and uninjured mucosa • Lab values can correlate poorly with coagulopathy • PT abnormal in 97% • aPTT abnormal in 70%

  27. Coagulopathy • Often present on admission esp. with CNS and penetrating trauma • Correlated with increased mortality • Often leads to further bleeding and ongoing need for volume resuscitation • Leads to further worsening of physiologic derrangments

  28. Bloody vicious cycle

  29. Normal clotting Tissue injury Exposure of tissue factor Activation of clotting cascade Local coagulation at wound

  30. Consumptive and Intravascular Coagulation Massive soft tissue damage, long bone fractures, CNS injury Systemic release of thromboplastin Systemic endothelial damage Widespread intravascular coagulation

  31. Dilutional Coagulopathy • Results from loss of whole blood and replacement of factor and platelet-poor fluids • ATLS 3:1 replacement of blood loss with crystalloid • Also in shock, fluid shifts from the extracellular to vascular space, worsening hemodilution

  32. Dilutional Coagulopathy • First described in 1954 • Commonly occurred in those receiving >10U of stored whole blood (up to 78%) • Related to stored platelet dysfunction and factor V and VIII deficiency • 1970’s: modified whole blood • Platelets removed • Thromobcytopenia related coagulopathy

  33. Dilutional Coagulopathy • 1980’s: fractionated component transfusion • Implemented to reduce infectious disease transmission and conserve scarce blood products • Diluted coagulation factors • Transfusion of components based on lab parameters (hgb>70, plt >30, INR>1.5)

  34. Dilutional Coagulopathy • Traditionally FFP transfusion started after 1 blood volume and/or INR>1.5 • Recommendations based on mathematical models in elective surgical patients • Drawbacks to previous recommendations • Mathematical models invalid in trauma pts • Relied on lab studies • Difficult to use clinically • Inadequate response

  35. FFP • One unit contains: • 0.5g fibrinogen • All other coagulation factors in physiologic concentrations • Will raise factors by 3–5% • Contains the most citrate of all blood products

  36. Slow paradigm shift to factor replacement before the development of coagulopathy • Now trending to replacement of RBC:plasma:platelets at 1:1:1 ratios

  37. Bloody vicious cycle

  38. Massive Transfusion Protocol • Implemented in June 2008 as a pilot • Developed by Trauma Services in conjunction with ER, ICU, OR, Transfusion Medicine and Canadian Blood services